Role of FcγRIII in the nasal cavity of BALB/c mice in the primary amebic meningoencephalitis protection model

Abstract

Different mechanisms of the host immune response against the primary amebic meningoencephalitis (PAM) in the mouse protection model have been described. It has been proposed that antibodies opsonize Naegleria fowleri trophozoites; subsequently, the polymorphonuclear cells (PMNs) surround the trophozoites to avoid the infection. FcγRs activate signaling pathways of adapter proteins such as Syk and Hck on PMNs to promote different effector cell functions which are induced by the Fc portion of the antibody-antigen complexes. In this work, we analyzed the activation of PMNs, epithelial cells, and nasal passage cells via the expression of Syk and Hck genes. Our results showed an increment of the FcγRIII and IgG subclasses in the nasal cavity from immunized mice as well as Syk and Hck expression was increased, whereas in the in vitro assay, we observed that when the trophozoites of N. fowleri were opsonized with IgG anti-N. fowleri and interacted with PMN, the expression of Syk and Hck was also increased. We suggest that PMNs are activated via their FcγRIII, which leads to the elimination of the trophozoites in vitro, while in the nasal cavity, the adhesion and consequently infection are avoided.

Identification of the Linear Fc-Binding Site on the Bovine IgG1 Fc Receptor (boFcγRIII) Using Synthetic Peptides

“…Recent studies have proven that in mouse natural killer cells, the receptors of CD16 and CD32b Fcγ are involved in regulating the antibody-mediated responses [ 31 ]. The Fc-FcγRIII engagement and alveolar macrophages are required for vaccine-induced antibody-mediated protection against antigen-shifted variants of SARS-CoV-2 as well as primary amebic meningoencephalitis in mouse models [ 32 , 33 ]. In a systemic lupus erythematosus (SLE) mouse model, the MRL/lpr mice treated with the Fc-binding peptide of huFcγRII showed the increased survival and reduce renal injury [ 34 ].…”